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Biomedical subjects

G C Curtis

Publications and source records attributed to G C Curtis.

At least 73 records · Page 4Linked to original sources
PubMed1982

The dexamethasone suppression test in panic disorder and agoraphobia.

Reports that imipramine and phenelzine prevent panic attacks in agoraphobia suggest the possibility that agoraphobia and/or panic disorder might be a clinical manifestation of underlying depression. To test this hypothesis, dexamethasone suppression tests (DSTs) were performed in 10 patients meeting DSM-III criteria for agoraphobia with panic attacks, 6 for panic disorder, and 4 whose diagnosis could have been either panic disorder or agoraphobia except that another axis I disorder precluded such a diagnosis. Abnormal DSTs were observed in only 3 patients and appeared to be attributable to causes other than panic attacks or agoraphobia. The results suggest that panic attacks and endogenous depression are separate disorders and that the antipanic properties of imipramine and phenelzine are separate from their antidepressant actions.

Adult↗
PubMed1981

Sensory experiences during treatment of phobias by in vivo exposure.

The author describes several patients undergoing in vivo exposure therapy for simple phobias who reported transient sensory distortions without other evidence of psychosis. The experiences occurred mainly in the tactile, kinesthetic, and visual modes. Their nature and significance are undetermined, but they appear to resemble conversion symptoms, hypnotic sensory distortions, and other nonpsychotic sensory experiences stimulated by emotionally charged ideas.

Adult↗
PubMed1980

Anxiety induced by flooding therapy for phobias does not elicit prolactin secretory response.

Eight subjects with severe phobias to insects and small animals had blood samples taken for measurement of prolactin concentration at regular intervals during five sessions of 3 hr duration each. Severe anxiety was induced by treating the phobia with in vivo flooding during the middle hour of the third and fourth sessions. Despite intense anxiety experienced by the subjects, they showed no change in plasma prolactin levels.

Anxiety↗
PubMed1980

Pretreatment nausea in cancer chemotherapy: a conditioned response?

Many patients receiving cancer chemotherapy become nauseated as they anticipate their treatments. We studied this phenomenon in eighteen cancer chemotherapy patients. The eight patients who reported pretreatment nausea had more extensive disease than the other patients and had received twice as much chemotherapy. In most cases pretreatment nausea developed only a after a number of months of treatment. Nausea was usually precipitated by the odor of the clinic and similar odors elsewhere also caused nausea. Patients continued to experience nausea during follow-up visits after treatment was completed. This syndrome of pretreatment nausea can be understood as a classically conditioned response. Clinical recommendations can be made on this basis.

Adult↗
PubMed1979

Plasma growth hormone: effect of anxiety during flooding in vivo.

The treatment of phobias by rapid in vivo exposure to the feared situation was accompanied by an increase in plasma growth hormone levels on at least one of two occasions in 8 of 11 subjects. The average growth hormone response was greater on the second occasion, even though subjective anxiety was less. Plasma growth hormone was not elevated during the subjects' adaptation to the laboratory. Strong subjective and behavioral anxiety responses failed to elevate plasma growth hormone levels in some subjects. The probability of a growth hormone response was the same whether or not baseline levels were elevated prior to exposure.

Adult↗
PubMed1978

Anxiety and plasma cortisol at the crest of the circadian cycle:reappraisal of a classical hypothesis.

Near-maximal anxiety by subjective and behavioral criteria was evoked and terminated in phobic patients by initiation and termination of rapid live confrontation ("flooding in vivo") with the specific stimulus that each avoided, at a time approximating the crest of the circadian cycle of adrenal cortical function. The procedure was associated with moderate, but not marked, elevations of plasma cortisol above control levels in some, but not all, subjects. Differences in anxiety levels as self-rated by the patients did not account for differences in cortisol response. The findings should stimulate further reevaluation of the hypothesis that affective arousal is the key psychological determinant of adrenal cortical function. Dissociation between subjective-behavioral arousal and plasma cortisol during flooding may be a manifestation of what behavior therapists call "desynchrony of fear."

Adult↗
PubMed1977

Paradoxical response to dopamine agonists in tardive dyskinesia.

The authors conducted an extensive pharmacological analysis of a patient severely affected by tardive dyskinesia. No drug treatment gave lasting clinical improvement. Several agents recently recommended for this condition, dimethyl aminoethanol, clozapine, and thioridazine, failed to modify the dyskinesia. Reserpine caused a worsening of the symptoms. A paradoxical and unexpected improvement was observed with apomorphine injections and with low-dosage oral L-dopa. These two drugs may have acted by stimulating presynaptic inhibitory dopamine receptors.

Adrenergic alpha-Agonists↗
PubMed1976

Neuroendocrine regulation in depression. I. Limbic system-adrenocortical dysfunction.

The regulation of hypothalamopituitary-adrenal (HPA) function in depressed patients was studied by a midnight dexamethasone suppression test. By using an observation period of 24 hours postadministration of dexamethasone, a graded series of abnormal test responses was identified. Depressed patients show abnormal early escape from suppression rather than absolute resistance to HPA suppression by dexamethasone. With increasing severity of depression, this escape occurs progressively more early on the day after administration of dexamethasone. These abnormalities were strongly related to the presence of HPA hyperactivity before dexamethasone was given. The essential disturbance of neuroendocrine regulation in depression is a failure of the normal brain inhibitory influence on the HPA system. This disinhibition of HPA activity suggests that there is an abnormal limbic system drive on the HPA axis in primary depressive illness.

Adrenal Glands↗
PubMed1976

Neuroendocrine regulation in depression. II. Discrimination of depressed from nondepressed patients.

Forty-two patients with endogenomorphic depression (ED) and 42 patients with other psychiatric disorders received an overnight dexamethasone test of hypothalamopituitary-adrenal (HPA) suppressibility. Plasma and urinary cortisol measures showed that the ED patients had significantly greater HPA activity before dexamethasone and less complete HPA suppression after dexamethasone. High cortisol vlaues after dexamethasone correlated strongly with spontaneous HPA disinhibition, as indicated by high baseline midnight plasma cortisol levels. Criteria for defining normal suppression responses were developed. All patients with depressive neuroses and most patients with other nondepressive disorders had completely normal responses to dexamethasone. About half of the ED patients had abnormal responses, whether or not they were receiving other drugs at the time of the test. Drug-free patients with depressive neuroses or other disorders showed no abnormal responses to dexamethasone. The effects of psychotropic drugs on the test require further study. Patients with two or more abnormal cortisol values after administration of dexamethasone were identified correctly as ED at confidence levels close to 100%. The dexamethasone suppression test may be of value as a laboratory aid in the diagnosis of "endogenous" depression.

Adrenal Glands↗
PubMed1976

Urinary free cortisol excretion in depression.

Urinary free cortisol (UFC) excretion was determined in 60 depressed inpatients and in 35 psychiatric inpatients with other disorders. The depressed patients had high daily UFC values, while the other patients excreted normal amounts. Over 40% of the depressed patients had UFC excretions in the range seen in Cushing's disease, while only 6% of the other patients excreted such high amounts of cortisol. Age and sex differences did not account for the results. Among the depressed patients those with depressive neuroses excreted less than unipolar or bipolar depressives. Following treatment, more normal UFC excretion was found in depressed patients. The estimation of UFC and its clinical utility are discussed in detail. UFC determination is a simple and informative indicator of adrenal cortical activation and its application to psychoendocrine studies is recommended.

Adjustment Disorders↗
PubMed1976

Cerebrospinal fluid and plasma free cortisol concentrations in depression.

Cerebrospinal fluid (CSF) cortisol levels were examined in a total group of 65 patients. Those who were not depressed (ND), and those suffering from depressive neuroses (DN) had marginally elevated values. Patients with unipolar depression (UD) and bipolar depression (BD) had levels twice as high as the ND and DN patients. Psychotic UD and BD patients had the highest values, three to four times as high as the ND and DN subjects. A significant reduction of CSF cortisol levels was observed following treatment and recovery. Manic patients had moderately elevated CSF cortisol values. The CSF results were in good agreement with plasma total cortisol levels and with urinary free cortisol excretion. Age and sex effects were not responsible for the observed differences; similar results were found in patient subgroups studied in Australia and in the United States. Preliminary equilibrium dialysis data are presented for plasma and CSF cortisol binding. CSF cortisol was 20% bound and 80% free. Plasma free cortisol levels were in good agreement with CSF free cortisol values. Depressed patients have increased tissue and central nervous system (CNS) exposure to free, physiologically active glucocorticoids. The appearance of severe depressive symptoms which manifest a diurnal rhythm may be determined in part by excesssve CNS exposure to glucocorticoids.

Adjustment Disorders↗
PubMed1976

Neuroendocrine identification of depressed patients.

Recent studies of hypothalamo--pituitary--adrenal (HPA) suppression in depressed patients indicate that these subjects often show abnormal early escape of plasma cortisol levels following an initial suppression. Non-depressed psychiatric inpatients usually show normal sustained HPA suppression. The responses of 49 depressed and 30 non-depressed patients have been analysed to develop criteria which can make the dexamethasone suppression test suitable for outpatient studies. The cortisol levels measured in a 24-hour urine collection and a single blood sample post-dexamethasone were sufficient to enable 61% of the depressed patients to be identified correctly at a confidence level of 90%, on the basis of at least one abnormal cortisol value. When both cortisol values were abnormal 35% of the depressed patient were identified correctly at a confidence level of 100%. Patients with "endogenous" depressive profiles had the most abnormal results. A normal response to this test will not necessarily exclude the diagnosis of primary depressive illness. An abnormal response to the test may be of help in confirming the diagnosis. With the simplified procedure outpatient studies may become possible.

Adjustment Disorders↗